Post-traumatic osteoarthritis (PTOA) is characterized by progressive articular cartilage erosion initiated by a variety of joint injuries ranging in severity from non-contact anterior cruciate ligament tears (ACLT) to intra-articular fracture (IAF). Even in the case of IAF, the immediate damage to cartilage and chondrocytes typically amounts to only a few percent of the joint surface. Yet, such localized lesions can expand over time; a phenomenon associated with release of mediators from injured cartilage. However, cartilage erosion also occurs away from originally damaged cartilage, indicating that catabolic factors carried in synovial fluid initiate degeneration in undamaged cartilage. Thus, an intervention centered on preventing trauma-induced inflammation holds great potential for reducing trauma-induced cartilage loss. Mechanical injuries to articular cartilage cause the death of chondrocytes and matrix degeneration in injury sites and, over time, in adjacent cartilage. Matrix fragments and cell debris signaling tissue damage (known collectively as